The fundamental enigma of crippling inflammatory injury to the lung is the identity of the mediators modulating the quantitative and topographical disposition of collagen. Mononuclear cells including monocytes, macrophages and lymphocytes are a basic histologic counterpart of many active fibrosing conditions. The importance of this association is signaled by recent observations that immunologically activated lymphocyte supernatants enhance collagenase release by macrophages and yet stimulate subpopulations of fibroblasts to accumulate collagen. The interrelationships of activated lymphocytes and monocytes will be explored in the proposed studies by tissue culture techniques which will aim to characterize 1) The fibroblast stimulating activity (ESA) of lymphokine preparations, its mode of action, its cellular source, and its effects upon differing fibroblastic cell strains. (2) The differences in monocyte mediators and lysosomal hydrolase production following differing methods of activation. 3) The integrated effects of combinations of lymphocyte and monocyte mediators upon the human lung fibroblast and its ability to accumulate collagen. The ultimate aim of these studies is the elucidation of contraveniny forces influencing collagen deposition in the lung with the hope that this knowledge will foster improved therapeutic approaches.